Current therapies to treat cancer involve, amongst other things, radiation therapy and chemotherapy each of which, although effective at retarding the growth of cancer cells, have significant disadvantages since each treatment is typically selective for cells that are actively dividing. Consequently, normal dividing cells are also destroyed resulting in significant undesirable side effects, such as nausea and immunosupression, the latter of which can lead to complications of secondary infections. In recent years research has focussed on providing selective treatments which lessen these undesirable side effects. One such therapy is GDEPT 1,2. 
GDEPT is of particular interest with respect to the treatment of cancer in that it offers advantages over conventional chemotherapeutic methods of cancer treatment. In such conventional methods the drugs administered to the patient attack not only the targeted cancer cells but also normal cells. Destruction of cancer cells is achieved at the expense of inflicting damage on normal cells, creating serious side-effects. In treatment of cancer by GDEPT the objective is to create an anti-cancer drug in situ within the cancer cell while creating little or none in normal cells, thereby attacking the cancer cells while leaving the normal cells substantially unaffected. This is typically achieved by administration to the patient of a vector containing a gene for an enzyme which can convert a relatively non-toxic substance (commonly referred to as a prodrug) into a cytotoxic agent. The vector also contains a promoter, ie a DNA sequence constituting a switch for the gene, this promoter being responsive to a regulatory protein found solely in the cancer cells or to a greater extent in the cancer cells than in normal cells. The gene is thus expressed substantially in the cancer cells so it is only (or mainly) in the cancer cells that the enzyme is produced and that conversion of the prodrug to the cytotoxic agent takes place. Formation of the cytotoxic agent therefore takes place primarily in the cancer cells. In this way the cancer cells are selectively attacked, with relatively little damage to normal cells.
In one example of the use of GDEPT in cancer treatment, the prodrug is 5-fluoro-cytosine (5-FC). 5-FC is itself relatively non-toxic to human cells but can be converted into a potent anti-cancer drug, 5-fluorouracil (5-FU), by the enzyme cytosine deaminase. A bacterial gene which expresses cytosine deaminase is incorporated in a viral vector in association with a promoter which is responsive to a regulatory protein that is characteristic of the particular type of cancer cell under attack. For instance, in treating breast cancer the promoter could be one which is responsive to the regulatory protein EBB2 or in treating liver cancer one which is responsive to α-fetoprotein.
In known GDEPT techniques, difficulty has been encountered in achieving as high a degree of selectivity as is desirable, (ie in destroying cancer cells while limiting the damage to normal cells). This is at least partly due to the fact that normal cells may come under attack from cytotoxic agents which have been formed in the cancer cells but have found their way out of those cells, for example when the cells break down under the cytotoxic action of the drug.
In addition, some chemotherapeutic agents are selective for particular cell-cycle phases (eg G1, S, G2 or mitosis). It is desirable to provide chemotherapeutic agents that are not so restricted in their effects and can kill cells irrespective of the cell-cycle stage.